miR-125a/b Regulates the Activation of Cancer Stem Cells in Paclitaxel-resistant Colon Cancer

Chen, Jixiang; Chen, Yuxiang; Chen, Zihua

doi:10.3109/07357907.2012.743557

Cited by 48 publications

(50 citation statements)

References 22 publications

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“…17 Several drugresistant cell lines have high levels of ALDH1A3, including A375 in melanoma and 1295Lu-resistant treated with temozolomide, taxol, or doxorubicin 18 and HT29-taxol resistant colon cancer cells. 19 The study shows downregulation of ALDH1A3 expression in pleural malignant mesotheliomas increased sensitivity to pemetrexed and cisplatin. 7 More details have been discussed elsewhere.…”

Section: Discussionmentioning

confidence: 99%

ALDH1A3 correlates with luminal phenotype in prostate cancer

et al. 2017

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Prostate cancer is the most common male malignancies in the United States. The specific characteristics of different disease stages have been deeply investigated. We present our data on ALDH1A3 as a potential therapeutic target for the prostate cancer based on several functional investigations. Also, we used The Cancer Genome Atlas datasets for primary prostate cancer to detect the relevance of ALDH1A3 and prostate cancer luminal phenotype. We found that ALDH1A3 correlated with androgen receptor signaling pathway in primary prostate cancer, which is consistent with its luminal layer localization. Then, from the genetic manipulation assay, we knocked out the ALDH1A3 in PC-3 cells and found significantly reduced proliferation rate as well as the invasion ability. Furthermore, we looked up our single center primary prostate cancer post-operative follow-up data and suggested that the high level ALDH1A3 expression could predict the poor progression-free survival in a 158-patient cohort. We concluded that ALDH1A3, localized in luminal layer in prostate epithelium, is highly expressed in prostate cancer. It played important role in maintaining the proliferation, invasion, and cell cycle. It can also become the potential biomarker in the future to guide the therapeutic manipulations for primary prostate cancer.

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Section: Discussionmentioning

confidence: 99%

ALDH1A3 correlates with luminal phenotype in prostate cancer

et al. 2017

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“…Emerging evidence has demonstrated that miRNAs are key regulators in the chemotherapeutic resistance of CRC. Ectopic expression of miR-125a/b restored paclitaxel sensitivity through downregulation of aldehyde dehydrogenase 1 in HT29 cells (20). Furthermore, Zhang et al (21) revealed that miR-587 promoted the resistance of CRC cells to 5-FU via inhibiting protein phosphatase 2 scaffold subunit Aβ.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of let‑7f‑5p promotes chemotherapeutic resistance in colorectal cancer by directly repressing several pro‑apoptotic proteins

et al. 2018

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Abstract. Colorectal cancer (CRC) is one of the most frequently occurring primary malignant tumors worldwide. Chemotherapeutic resistance is a major clinical problem in the treatment of CRC. Therefore, it is of great importance to investigate novel biomarkers that may predict chemoresistance and facilitate the development of individualized treatment for patients with CRC. The present study reported that let-7f-5p expression was elevated in chemotherapy-resistant CRC tissues compared with chemotherapy-sensitive tissues. Furthermore, upregulating let-7f-5p increased the expression levels of the anti-apoptotic proteins, B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL), and decreased the activity of caspase-3 and caspase-9 in CRC cells. By contrast, downregulating let-7f-5p yielded the opposite effect. Notably, the results indicated that let-7f-5p promoted chemotherapeutic resistance by directly repressing the expression of several pro-apoptotic proteins, including tumor protein p53, tumor protein p53-inducible nuclear protein 1, tumor protein p53-inducible nuclear protein 2 and caspase-3. Therefore, a novel mechanism by which let-7f-5p enhances the resistance of CRC cells to chemotherapeutics has been revealed, indicating that silencing let-7f-5p may become an effective therapeutic strategy against CRC. IntroductionColorectal cancer (CRC) is one of the most prevalent causes of cancer-associated mortality worldwide (1,2). Clinically, 5-fluorouracil (5-FU)-based chemotherapy serves as the initial first-line chemotherapeutic drug of choice in patients with CRC; however, the response rates to 5-FU are ~15% in patients with advanced CRC (3). Although novel therapeutic approaches, including combination chemotherapy of 5-FU and oxaliplatin (FOLFOX) or irinotecan (FOLFIRI), have presented promising potential, the majority of the patients continue to exhibit inadequate responses (4,5). The failure of chemotherapy in CRC patients is primarily attributed to therapeutic resistance following a long period of treatment (6). These observations emphasize that chemotherapeutic resistance is a major obstacle in the treatment of CRC, and that the molecular mechanisms underlying this issue remain unclear.Chemotherapeutic resistance poses a major challenge in cancer chemotherapy. Chemoresistance of tumor cells develops primarily due to acquired resistance de novo, following an initially sensitive response, and/or in combination with pre-established cell-intrinsic mechanisms (7). A number of well-established mechanisms are reported to be involved in cancer drug resistance, including failure of the drug to reach or enter the target cell, formation of efflux pumps on the surface of tumor cells, increased expression of anti-apoptotic proteins, induction of drug-detoxifying mechanisms and upregulation of DNA repair enzymes (8,9). However, there is an absence of integral understanding of acquired drug resistance in the context of CRC. Such insight may be crucial for the

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“…21,22 Studies have shown that MCL1 expression is upregulated in B-cell lymphomas, chronic myeloid leukemia, multiple myeloma, lung cancer, cholangiocarcinoma, and hepatocellular carcinoma; this upregulation contributes to cancer cell survival, chemoresistance, and disease relapse. 10,13,14,16,23,24 Overexpression of MCL1 was demonstrated to be associated with a poor prognostic outcome in several tumors, including myeloma, breast cancer, and leukemia. 25 Also, in colon cancer, MCL1 expression was reportedly increased in adenoma and carcinoma tissues compared with normal colonic epithelium.…”

Section: Discussionmentioning

confidence: 99%